1.11 Drugs and the Peripheral NS Flashcards
How does the PNS breakdown?
PNS to motor and sensory NS
Motor to somatic and autonomic
autonomic to sympathetic and parasympathetic
Which NS uses:
1) efferent nn fibres
2) afferent nn fibres
1) Sensory
2) motor`
Which break down of motor NS is
1) voluntary
2) involuntary
1) somatic
2) autonomic
What happens to the following in
1) sympathetic innervation
2) parasympathetic innervation
a) pupils
b) lens of eye adjusts for ___ vision
1) Pupils dilate (peripheral vision)
b) far
2) Pupils constrict
b) closer
What happens to the following in
1) sympathetic innervation
2) parasympathetic innervation
a) HR
b) Blood vessels to limbs
c) to visceral organs
d) brain activity
1) Heart rate increases Blood vessels to limb muscles dilate Blood vessels to visceral organs constrict Brain activity general alertness 2) Heart rate decrease Blood vessels to limb muscles constrict Blood vessels to visceral organs more dilated Brain activity normalise
What happens to the following in
1) sympathetic innervation
2) parasympathetic innervation
a) Respiratory rate
b) salivary secretions
1) a) increases
b) reduced
2) a) decreases
b) increased
a) What neurotransmittor is used at the following junctions in sympathetic NS
1) preganglionic
2) postganglionic
b) What are the exceptions to this rile
a) 1) ACh (acetyl choline)
2) NA (noradrenaline)
b) sweat glands everything is ACh and , adrenal medulla, ACh causes secretionb of adrenaline into the blood.
a) What neurotransmittor is used at the following junctions in parasympathetic NS
1) preganglionic
2) postganglionic
b) At neuromuscular junctions in somatic what neurotransmittor is used
a) 1) ACh
2) ACh
b) ACh!!
(acetyl choline)
Describe synthesis of Acetyl choline at junctions:
i.e. enzyme and substrates
choline/choline acetyl transferase (CAT) is the synthetic anexyme, formed from choline and AcCoA
Describe storage of Acetyl choline at junctions:
2) WhY?
vesicles
2) prevent degradation
Describe release of Acetyl choline at junctions:
exocytosis into synapse
Describe receptor interactions of Acetyl choline at junctions:
binds to a muscarinic or a nicotinic receptor
Describe termination of Acetyl choline at junctions:
broken down in synapse by acetylcholine esterase (degradation enzyme)
The actions of ACh are mediated via 2 main classes of ACh receptor
Names:
Muscarinic receptors
Nicotinic receptors
1) What are the subclasses of muscarinic receptor?
2) What type of receptor is it ?
3) Where is the receptor located within the body?
4) response time compared to nicotinic?
1) M1,2,3,
2) G protein coupled
3) Located at postganglionic parasympathetic synapses
(found at target organ/ effector tissue)
4) slow (seconds)
Nicotinic receptors (nACh), What are the 2 main receptor subtypes: (excitatory? or inhibitory?)
b) what type of receptor is it?
c) Where is it located?
d) response time compated to muscarinic:
muscle-type: neuromuscular junction (NMJ) (excitatory)
2) neuronal type- brain and autonomic ganglia (excitatory)
b) Ligand gated ion channels (or ionotropic receptor)
c) Located in ganglia and on NMJ ( preganglionic and in muscles(“only” target mm found in))
Fill spaces:
• Muscarinic receptors are just located in A.
• Nicotinic neuronal type are involved in B
• Nicotinic muscle type are involved in C
A) parasympathetic system,
B) parasympathetic and sympathetic system.
C) somatic effects.
Knowing muscarinic receptors are involved in the parasympathetic system. What effect does a muscarinic A)agonist and B) antagonist have on:
1) pupillary muscle in pupil
2) focal length of lens (ciliary mm)
3) bronchioles
A) 1) increases pupil constriction (contraction)
2) decreases focal length (contracts)
3)Bronchoconstriction
B) the opposite
Knowing muscarinic receptors are involved in the parasympathetic system. What effect does a muscarinic A)agonist and B) antagonist have on:
1) cardiac output (=HR*SV(force))
2) GI motility
3) exocrine gland secretion (sweating, salivation, bronchiol secretion)
C) Whats wrong with this?
A)1) decrease 2) increases 3) increases B) the opposite C) sweating is actually a sympathetic effect
1) What are muscarinic agonists know as ?
2) Why?
3) What are muscarinic antagonists known as ?
1) as parasympathomimetics
2) they stimulate muscarinic receptors
3) as parasympatholytic .
Considering the effects of antagonist muscarinic receptors what are they used for get a few:
pupil dilation in eye surgery , decrease oral /respiratory secretions before oral procedures and as an adjunct to anaesthesia (as when your on ventilator you don’t have cough reflex), resuscitation in bradycardia, asthma patients , GI motility= motion sickness
Considering the effects of agonist muscarinic receptors what are they used for get a few:
1) how does it treat glaucoma (build of lfui din the eye)
2) the oral condition it treats
a) how is it taken
b) side effects
1) focus on near vision + also allows increase drainage of aqueous humour
Contraction of sphincter muscle causes pupil constriction
2) xerostomia: stimulates saliva secretions
a) Taken systemically
b) Side effects: muscarinic-sweating, nausea, minimal cardiovascascular side effect (due to low dose)
Treatment for :
1) asthma
2) Xerostomia
3) Motion sickness (decrease gastric motility)
4) Bradycardia
muscarinic antagonist: 1,3, 4
muscarinic agonist: 2
Treatment for :
1) to decrease secretions
2) pupil dilation in eye surgery
3) glaucoma
muscarinic antagonist: 1,2,
muscarinic agonist: 3
What is the effect of nicotinic antagonists?
loss of sympathetic & parasympathetic reflexes, especially cardiac
What is the effect of nicotinic agonists targeting nicotinic receptors found at NMJ?
2) What is the importance of this in medicine when agonist is SYNTHETIC:
3) What does it cause?
4) used when?
Stimulation of these receptors by ACh causes depolarisation (in muscle fibre this is known as an end plate potential (EPP)) and contraction of the skeletal muscle fibre
2) Because the synthetic agonist is not metabolised rapidly by acetylcholinesterase, the fibre is persistently depolarised resulting in loss of further electrical excitability-known as depolarising block
3) depolarising block
4) paralysis/ muscle relaxation (for surgery)
nicotinic agonists or antagonstic cause :
1) depolarising block
2) non-depolarising block
b) why?
c) What do they both have in common?
1) agonist b)synthetic agonist is not metabolised rapidly by acetylcholinesterase,fibre is persistently depolarised resulting in loss of further electrical excitability-known as depolarising block
2) antagonist b) Hyperpolarisation, inhibition of EPPs (initial depolarisation)
Muscle fibre relaxation
c) both cause paralysis (used in surgery)
What is anticholinesterases used to for? (2)
Myasthenia gravis
Induce paralysis for surgery
what is used to treat myasthenia gravis?
2) how does it work?
3) What is this disease?
1) anticholinesterases
2) inhibits acetylcholinesterase, thus ACh not metabolised nad action not terminated, amount of ACh isecreted increase therefore can have greater effect. Too much and can be harmful
3) (autoimmune disease, circulating antibodies against muscle nicotinic receptors)
